It has been suggested that the perfusion pressure to the kidney may be an important regulator of renal sodium excretion. Utilizing both an in situ rat kidney and an isolated, perfused rat kidney we propose to further define the relationship between renal sodium transport and an acute increase in renal perfusion pressure. Specifically, these studies will examine: 1) whether the natriuretic effect of an acute increase in renal perfusion pressure is due to a decrease in sodium reabsorption in inner cortical nephrons or to an alteration in net sodium transport in the papillary collecting duct; 2) changes in the quantity and distribution of renal blood flow and glomerular filtration which occur following an acute increase in the renal perfusion pressure; 3) the hydrostatic and oncotic pressure in the vasa recta prior to and following an acute elevation in the renal perfusion pressure. The prostaglandin, PGE2, is one of the prostaglandins formed within the kidney. As such, it is not unreasonable to assume that it may have important physiologic roles within the kidney. As this prostaglandin may play an important role in the regulation of renal sodium excretion, with the use of micropuncture techniques we propose to determine the direct influence of PGE2 on sodium reabsorption in the superficial proximal and distal convoluted tubule of the rat nephron.